Is there any evidence that cerebral protection is beneficial? Experimental data

This article presents the available experimental data from the world literature on the use of cerebral protection devices during carotid artery stenting (CAS). Clinical studies relying on surrogate markers of cerebral embolisation in place of neurological event rate as primary outcome measures are evaluated alongside bench-top and animal studies. These surrogate markers include evaluations of outcomes using procedural transcranial Doppler (TCD) and diffusion-weighted magnetic resonance imaging of brain (DWI). Pathological analyses of debris retrieved from in-vivo analyses of protection devices are also included in this review because although the focus of these studies was primarily clinical, the laboratory data will be preferentially presented and it provides interesting insights. It can be shown that each of the three philosophies of cerebral protection, namely flow arrest (proximal or distal), flow reversal and distal filtration is capable of the entrapment of sizeable debris that would logically threaten devastating stroke if it embolized to the brain. Whilst balloon occlusion significantly reduces the procedural microembolic load (particles less than 60 mm) and flow reversal may be the first means to entirely eliminate it, filters may be associated with increased microembolization. This has been described by some workers as controlled embolization. Certainly, particles smaller than the pore size of currently available filters (60-140 mm) will readily evade capture due to filter periflow and through-flow. There is evidence to suggest that tens of thousands of particles of this size may be released during CAS and there is some evidence that this may be associated with more new white lesions on DWI of brain. The clinical consequences of this controlled embolization however, remain unclear and sophisticated neuropsychometric test batteries may need to be applied at later time points to detect subtle injury that may be compounded by a late inflammatory response around cerebral emboli. Devices relying on placement in the distal internal carotid artery (ICA) for establishment of protection risk intimal damage and the release of microemboli due largely to device deployment and retrieval. Although devices effecting flow arrest and flow reversal will limit all embolization, they do so at the expense of constant procedural cerebral perfusion and may not be tolerated in patients with precarious cerebral reserve capacity, loss of integrity of the Circle of Willis and/or high-grade stenosis of the contralateral ICA. Advances in the concept of cerebral protection will require technical refinements to existing devices, alternative mechanical strategies and/or pharmacological plaque stabilization.